Mitochondria buffer Ca2+ entry but not intracellular Ca2+ release in mouse DRG neurones.
Mitochondrial Ca2+ pool was investigated in dorsal root ganglion neurones acutely isolated from 4-5 week old mice. Under the resting conditions application of mitochondrial protonophore CCCP triggered a slight increase in [Ca2+]i. In contrast, application of CCCP during the plateau phase of KCl-induced [Ca2+]i transient triggered large elevation in [Ca2+]i. In the presence of CCCP the amplitude of depolarization-induced [Ca2+]i elevation significantly increased, whereas the plateau phase of [Ca2+]i transient disappeared. On the contrary, CCCP failed to modulate [Ca2+]i transients resulting from caffeine-induced Ca2+ release. We concluded that mitochondrial Ca2+ pool distinguished the origin of Ca2+ ions entering the cytoplasm: it effectively buffers Ca2+ entering the cell through plasmalemmal channels but fails to regulate [Ca2+]i transients resulting from Ca2+ release from ER Ca2+ stores possibly due to peculiar localization of mitochondria far away from the Ca2+ release sites.
Svichar
N
N
Bogomoletz Institute of Physiology and International Center of Molecular Physiology, Kiev, Ukraine.
Kostyuk
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P
Verkhratsky
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A
D000818:Animals; D002021:Buffers; D002110:Caffeine / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D000697:Central Nervous System Stimulants / Q000494:pharmacology; D005727:Ganglia, Spinal / Q000166:cytology / Q000378:metabolism*; D008564:Membrane Potentials / Q000502:physiology; D051379:Mice; D008928:Mitochondria / Q000378:metabolism*; D009474:Neurons / Q000378:metabolism*
D002021:Buffers; D000697:Central Nervous System Stimulants; D002110:Caffeine; D002118:Calcium